Postpartum lactation in humans and monkeys is associated with ovarian quiescence attributed to suckling-induced deficits in GnRH secretion and hyperprolactinemia. The work proposed in this application would investigate the validity and nature of these mechanisms in the rhesus monkey, a primate in which the control of gonadotropin secretion and ovarian function appear similar to the human. 1. Because a reduced frequency of pulsatile GnRH release has the potential of disrupting normal gonadotropin secretion and ovarian cycles, the intermittent discharge of this hypothalamic hormone will be assessed indirectly by measuring pulsatile LH release in chronically catheterized monkeys nursing their infants. Moreover, changes in pulsatile LH release that might occur following abrupt removal of the infant will be recorded at several postpartum intervals. To relate the intensity of the suckling stimulus to the duration of gonadotropin suppression during lactation, some rhesus infants will be retricted to mother's milk during the usual period of weaning in an attempt to delay resumption of maternal pituitary function as assessed by pulsatile LH secretion and the positive feedback action of estradiol. 2. The possibility that the sensitivity of the hypothalamic-pituitary axis to the negative feedback action of estrogen is enhanced during lactation will be tested in ovariectomized monkeys bearing estradiol capsules that produce low circulating levels of the steroid. 3. Exogenous pulses of GnRH will be administered to nursing monkeys in an attempt to re-initiate pituitary and ovarian function. Moreover, the possible role of progesterone in mediating the inhibitory action of lactational hyperprolactinemia on ovarian follicular development will be investigated in monkeys with hypothalamic lesions receiving pulsatile GnRH replacement and progesterone capsules. 4. The central neural mechanisms underlying the inhibition of GnRH secretion in lactating monkeys will be studied by measuring pulsatile LH release during suckling following administration of antagonists to the endogenous opioid peptides, dopamine, and serotonin. These studies, which are difficult to perform under suitable controlled conditions in humans, will serve to delineate the mechanisms involved in lactational amenorrhea in a primate model.